pubmed-article:7696505 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7696505 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
pubmed-article:7696505 | lifeskim:mentions | umls-concept:C0019564 | lld:lifeskim |
pubmed-article:7696505 | lifeskim:mentions | umls-concept:C0034830 | lld:lifeskim |
pubmed-article:7696505 | lifeskim:mentions | umls-concept:C0031164 | lld:lifeskim |
pubmed-article:7696505 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:7696505 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:7696505 | pubmed:dateCreated | 1995-5-4 | lld:pubmed |
pubmed-article:7696505 | pubmed:abstractText | The hippocampal nicotinic acetylcholine receptor (nAChR) is a newly identified ligand-gated ion channel that is blocked by the snake toxin alpha-bungarotoxin (alpha-BGT) and that probably contains the alpha 7 nAChR subunit in its structure. Here its ion selectivity was characterized and compared with that of the N-methyl-D-aspartate (NMDA) receptor channel. The reversal potentials (VR) of acetylcholine- and NMDA-activated whole-cell currents were determined under various ionic conditions. Using ion activities and a Goldman-Hodgkin-Katz equation for VR shifts in the presence of Ca2+, permeability ratios were calculated. For the alpha-BGT-sensitive nAChR, PNa/PCs was close to 1 and Cl- did not contribute to the currents. Changing the [Ca2+]0 from 1 to 10 mM, the VRs of the nAChR and NMDA currents were shifted by +5.6 +/- 0.4 and +8.3 +/- 0.4 mV, respectively, and the nAChR current decay was accelerated. These shifts yielded PCa/PCss of 6.1 +/- 0.5 for the nAChR channel and 10.3 +/- 0.7 for the NMDA channel. Thus, the neuronal alpha-BGT-sensitive nAChR is a cation channel considerably selective to Ca2+ and may mediate a fast rise in intracellular Ca2+ that would increase in magnitude with membrane hyperpolarization. | lld:pubmed |
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pubmed-article:7696505 | pubmed:language | eng | lld:pubmed |
pubmed-article:7696505 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7696505 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7696505 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7696505 | pubmed:month | Feb | lld:pubmed |
pubmed-article:7696505 | pubmed:issn | 0006-3495 | lld:pubmed |
pubmed-article:7696505 | pubmed:author | pubmed-author:AlbuquerqueE... | lld:pubmed |
pubmed-article:7696505 | pubmed:author | pubmed-author:CastroN GNG | lld:pubmed |
pubmed-article:7696505 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7696505 | pubmed:volume | 68 | lld:pubmed |
pubmed-article:7696505 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7696505 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7696505 | pubmed:pagination | 516-24 | lld:pubmed |
pubmed-article:7696505 | pubmed:dateRevised | 2010-9-13 | lld:pubmed |
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pubmed-article:7696505 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:7696505 | pubmed:articleTitle | alpha-Bungarotoxin-sensitive hippocampal nicotinic receptor channel has a high calcium permeability. | lld:pubmed |
pubmed-article:7696505 | pubmed:affiliation | Department of Pharmacology and Experimental Therapeutics, University of Maryland School of Medicine, Baltimore 21201-1559. | lld:pubmed |
pubmed-article:7696505 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7696505 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:7696505 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:7696505 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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